FIGURE 6.

An overview diagram illustrating the role of senescence, brain inflammation, and TauO in AD and potential therapeutic targets. Various risk factors, including aging, can trigger senescence, inflammation, and TauO production, resulting in impaired synaptic and neuronal function loss, which are essential for learning and memory. This also induces the release of HMGB1 and initiates the SASP which lead to Aβ and tau pathology, proteasomal dysfunction, glial dysfunctions, mitochondrial dysfunctions, impaired BBB, synaptic and neuronal loss. Senescence, brain inflammation, and TauO can interact with each other and contribute to AD pathogenesis through several mechanisms. For example, TauO can trigger senescence and inflammation in the brain, which can impair the clearance of TauO and promote their aggregation and propagation. Senescence and inflammation can also impair the BBB functions, allowing more peripheral inflammatory factors to enter the brain and worsen neurodegeneration. Therefore, targeting senescence, inflammation, and TauO in combination may be a promising therapeutic strategy for AD. Aβ, amyloid beta; AD, Alzheimer's disease; BBB, blood‐brain barrier; SASP, senescence‐associated secretory phenotype; TauO, tau oligomers.